Evidence map›Paper›PMID 25810907›Full record

ArticleCancer & metabolism2015

Mitophagy and cancer.

Aparajita H Chourasia, Michelle L Boland, Kay F Macleod

Abstract read
In one paragraph

Article in Cancer & metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

155 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Guideline
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  3. Article
  4. [NPLOC4 promotes proliferation, invasion, and migration of hepatocellular carcinoma cells via enhancing Wnt/Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Article
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  7. Review
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  16. Article
  17. Translational lung cancer research · 2025
    Article
  18. Article
  19. Review
  20. Article

95 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Aparajita H ChourasiaThe Ben May Department for Cancer Research, The University of Chicago, 929 East 57th Street, Chicago, IL 60637 USA ; The Committee on Cancer Biology, The University of Chicago, 929 East 57th Street, Chicago, IL 60637 USA.
Michelle L BolandThe Ben May Department for Cancer Research, The University of Chicago, 929 East 57th Street, Chicago, IL 60637 USA ; The Committee on Molecular Metabolism & Nutrition, 929 East 57th Street, Chicago, IL 60637 USA.
Kay F MacleodThe Ben May Department for Cancer Research, The University of Chicago, 929 East 57th Street, Chicago, IL 60637 USA ; The Committee on Cancer Biology, The University of Chicago, 929 East 57th Street, Chicago, IL 60637 USA ; The Committee on Molecular Metabolism & Nutrition, 929 East 57th Street, Chicago, IL 60637 USA ; The Ben May Department for Cancer Research, The University of Chicago Comprehensive Cancer Center, The Gordon Center for Integrative Sciences, W338 929 East 57th Street, Chicago, IL 60637 USA.

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Multi-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5M
Autophagy in Tumor Progression and MetastasisR01CA162405 · NCI · UNIVERSITY OF CHICAGO · PI MACLEOD, KAY F · 2012 to 2016
$1.6M
Functions of BNIP3 in Mammary TumorigenesisR01CA131188 · NCI · UNIVERSITY OF CHICAGO · PI MACLEOD, KAY F · 2009 to 2013
$1.5M
Re-Engineering Translational Research at the University of ChicagoTL1TR000432 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$289k
NCATS NIH HHS TL1 TR000432NCATS NIH HHS UL1 TR000430NCI NIH HHS R01 CA131188NCI NIH HHS R01 CA162405NCI NIH HHS T32 CA009594
6 · The paper itself

Abstract

Mitophagy is a selective form of macro-autophagy in which mitochondria are selectively targeted for degradation in autophagolysosomes. Mitophagy can have the beneficial effect of eliminating old and/or damaged mitochondria, thus maintaining the integrity of the mitochondrial pool. However, mitophagy is not only limited to the turnover of dysfunctional mitochondria but also promotes reduction of overall mitochondrial mass in response to certain stresses, such as hypoxia and nutrient starvation. This prevents generation of reactive oxygen species and conserves valuable nutrients (such as oxygen) from being consumed inefficiently, thereby promoting cellular survival under conditions of energetic stress. The failure to properly modulate mitochondrial turnover in response to oncogenic stresses has been implicated both positively and negatively in tumorigenesis, while the potential of targeting mitophagy specifically as opposed to autophagy in general as a therapeutic strategy remains to be explored. The challenges and opportunities that come with our heightened understanding of the role of mitophagy in cancer are reviewed here.

Indexed as

AutophagosomesBNIP3Mitochondrial dysfunctionMitophagyNIXParkin

Identifiers

PMID25810907
PMCPMC4373087

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.